Repetitive restriction of muscle blood flow enhances mTOR signaling pathways in a rat model

2016 ◽  
Vol 31 (10) ◽  
pp. 1685-1695 ◽  
Author(s):  
Toshiaki Nakajima ◽  
Tomohiro Yasuda ◽  
Seiichiro Koide ◽  
Tatsuya Yamasoba ◽  
Syotaro Obi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Signaling Pathways ◽  
Rat Model ◽  
Muscle Blood Flow ◽  
Mtor Signaling

A study of regional gastric mucosal blood flow in a rat model of hepatic cirrhosis

1992 ◽  
Vol 262 (4) ◽  
pp. G727-G731 ◽  
Author(s):  
J. G. Geraghty ◽  
W. J. Angerson ◽  
D. C. Carter
Keyword(s):  
Blood Flow ◽  
Rat Model ◽  
Hepatic Cirrhosis ◽  
Muscle Blood Flow ◽  
Gastric Wall ◽  
Regional Distribution ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Experimental Cirrhosis ◽  
Significant Difference

There is controversy surrounding the effects of portal hypertension on the level of perfusion to the gastric wall. This study maps the regional distribution of gastric mucosal and muscle blood flow measured using quantitative autoradiography in a carbon tetrachloride-induced rat model of hepatic cirrhosis. There was a significant increase in both corpus mucosal (124.3 +/- 13.8 vs. 84.8 +/- 4.2 ml.100 g-1.min-1) and muscle blood flow (50.9 +/- 3.6 vs. 33.4 +/- 2.3 ml.100 g-1.min-1) in animals with experimental cirrhosis compared with controls. There was no significant difference in the ratio of blood tracer concentration between the basal and luminal aspects of corpus mucosa in cirrhotic and control groups. We conclude that experimental cirrhosis is associated with gastric mucosal hyperperfusion and that "active" rather than "passive" congestion of the stomach wall may be a more appropriate description of the basic hemodynamic change in this model.

scholarly journals Exercising Skeletal Muscle Blood Flow is Diminished in a Rat Model of Pulmonary Arterial Hypertension

2019 ◽  
Vol 51 (Supplement) ◽  
pp. 614
Author(s):  
Gary M. Long ◽  
Andrea Frump ◽  
Ashley Troutman ◽  
Melissa Mailand ◽  
Kaylee Ann Ellis ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Rat Model ◽  
Muscle Blood Flow ◽  
Skeletal Muscle Blood Flow ◽  
Pulmonary Arterial

scholarly journals Mechanisms of rapid vasodilation after a brief contraction in human skeletal muscle

2013 ◽  
Vol 305 (1) ◽  
pp. H29-H40 ◽  
Author(s):  
Anne R. Crecelius ◽  
Brett S. Kirby ◽  
Gary J. Luckasen ◽  
Dennis G. Larson ◽  
Frank A. Dinenno
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Signaling Pathways ◽  
Muscle Blood Flow ◽  
Maximum Voluntary Contraction ◽  
Area Under The Curve ◽  
Voluntary Contraction ◽  
Impact Peak ◽  
Inwardly Rectifying

A monophasic increase in skeletal muscle blood flow is observed after a brief single forearm contraction in humans, yet the underlying vascular signaling pathways remain largely undetermined. Evidence from experimental animals indicates an obligatory role of vasodilation via K+-mediated smooth muscle hyperpolarization, and human data suggest little to no independent role for nitric oxide (NO) or vasodilating prostaglandins (PGs). We tested the hypothesis that K+-mediated vascular hyperpolarization underlies the rapid vasodilation in humans and that combined inhibition of NO and PGs would have a minimal effect on this response. We measured forearm blood flow (Doppler ultrasound) and calculated vascular conductance 10 s before and for 30 s after a single 1-s dynamic forearm contraction at 10%, 20%, and 40% maximum voluntary contraction in 16 young adults. To inhibit K+-mediated vasodilation, BaCl2 and ouabain were infused intra-arterially to inhibit inwardly rectifying K+ channels and Na+-K+-ATPase, respectively. Combined enzymatic inhibition of NO and PG synthesis occurred via NG-monomethyl-l-arginine (l-NMMA; NO synthase) and ketorolac (cyclooxygenase), respectively. In protocol 1 ( n = 8), BaCl2 + ouabain reduced peak vasodilation (range: 30–45%, P < 0.05) and total postcontraction vasodilation (area under the curve, ∼55–75% from control) at all intensities. Contrary to our hypothesis, l-NMMA + ketorolac had a further impact (peak: ∼60% and area under the curve: ∼80% from control). In protocol 2 ( n = 8), the order of inhibitors was reversed, and the findings were remarkably similar. We conclude that K+-mediated hyperpolarization and NO and PGs, in combination, significantly contribute to contraction-induced rapid vasodilation and that inhibition of these signaling pathways nearly abolishes this phenomenon in humans.

scholarly journals Abnormal skeletal muscle blood flow, contractile mechanics and fibre morphology in a rat model of obese‐HFpEF

2021 ◽  
Author(s):  
Ever Espino‐Gonzalez ◽  
Peter G. Tickle ◽  
Alan P. Benson ◽  
Roger W. P. Kissane ◽  
Graham N. Askew ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Rat Model ◽  
Muscle Blood Flow ◽  
Skeletal Muscle Blood Flow ◽  
Fibre Morphology

Measurement of Renal Blood Flow by 131I-Labelled Sodium Iodohippurate Imaging in a Rat Model of Herpes Encephalitis

1990 ◽  
Vol 31 (5) ◽  
pp. 538-539
Author(s):  
G. M. Cleator ◽  
P. E. Klapper ◽  
A. G. Lewis ◽  
H. L. Sharma ◽  
A. M. Smith
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Rat Model ◽  
Herpes Encephalitis

Exploration of the Effect and Mechanism of ShenQi Compound in a Spontaneous Diabetic Rat Model

2019 ◽  
Vol 19 (5) ◽  
pp. 622-631 ◽  
Author(s):  
Ya Liu ◽  
Jian Kang ◽  
Hong Gao ◽  
Xiyu Zhang ◽  
Jun Chao ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Signaling Pathway ◽  
Rat Model ◽  
Mtor Signaling ◽  
Diabetic Rat ◽  
Gene Microarray ◽  
Mtor Signaling Pathway ◽  
Glucose Fluctuation ◽  
Blood Glucose Fluctuation ◽  
Diabetic Rat Model

Background: Type 2 Diabetes Mellitus (T2DM) is a world-wide metabolic disease with no cure from drugs and treatment. In China, The Traditional Chinese Medicine (TCM) herbal formulations have been used to treat T2DM for centuries. Methods: In this study, we proposed a formula called ShenQi Compound (SQC), which has been used in clinical therapeutics in China for several years. We evaluated the effect of SQC in a spontaneous diabetic rat model (GK rats) by detecting a series of blood indicators and performing histological observations. Meanwhile, the gene microarray and RT-qPCR experiments were used to explore the molecular mechanism of SQC treatment. In addition, western medicine, sitagliptin was employed as a comparison. Results: The results indicated that SQC and sitagliptin could effectively improve the serum lipid (blood Total Cholesterol (TC) and blood Triglycerides (TG)), hormone levels (serum insulin (INS), Glucagon (GC) and Glucagon-Like Peptide-1 (GLP-1)), alleviated the inflammatory response (hypersensitive C-Reactive Protein (hsCRP)), blood glucose fluctuation (Mean Blood Glucose (MBG), standard deviation of blood glucose (SDBG) and Largest Amplitude of plasma Glucose Excursions (LAGE)), pancreatic tissue damage and vascular injury for T2DM. Compared with sitagliptin, SQC achieved a better effect on blood glucose fluctuation (p<0.01). Meanwhile, the gene microarray and RT-qPCR experiments indicated that SQC and sitagliptin may improve the T2DM through affecting the biological functions related to apoptosis and circadian rhythm. Moreover, SQC might be able to influence the mTOR signaling pathway by regulating Pik3r1, Ddit4 expression. Conclusion: All these results indicate that SQC is an effective therapeutic drug on T2DM. Notably, SQC presents an obvious blood glucose fluctuation-preventing ability, which might be derived from the regulation of the mTOR signaling pathway.

Neural control of glucose uptake by skeletal muscle after central administration of NMDA

1995 ◽  
Vol 268 (2) ◽  
pp. R492-R497 ◽  
Author(s):  
C. H. Lang ◽  
M. Ajmal ◽  
A. G. Baillie
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Glucose Uptake ◽  
Neural Control ◽  
Plasma Insulin ◽  
Regional Blood Flow ◽  
Muscle Blood Flow ◽  
Whole Body ◽  
Glucose Disposal ◽  
Central Administration

Intracerebroventricular injection of N-methyl-D-aspartate (NMDA) produces hyperglycemia and increases whole body glucose uptake. The purpose of the present study was to determine in rats which tissues are responsible for the elevated rate of glucose disposal. NMDA was injected intracerebroventricularly, and the glucose metabolic rate (Rg) was determined for individual tissues 20-60 min later using 2-deoxy-D-[U-14C]glucose. NMDA decreased Rg in skin, ileum, lung, and liver (30-35%) compared with time-matched control animals. In contrast, Rg in skeletal muscle and heart was increased 150-160%. This increased Rg was not due to an elevation in plasma insulin concentrations. In subsequent studies, the sciatic nerve in one leg was cut 4 h before injection of NMDA. NMDA increased Rg in the gastrocnemius (149%) and soleus (220%) in the innervated leg. However, Rg was not increased after NMDA in contralateral muscles from the denervated limb. Data from a third series of experiments indicated that the NMDA-induced increase in Rg by innervated muscle and its abolition in the denervated muscle were not due to changes in muscle blood flow. The results of the present study indicate that 1) central administration of NMDA increases whole body glucose uptake by preferentially stimulating glucose uptake by skeletal muscle, and 2) the enhanced glucose uptake by muscle is neurally mediated and independent of changes in either the plasma insulin concentration or regional blood flow.

Muscle maximal O2 uptake at constant O2 delivery with and without CO in the blood

1990 ◽  
Vol 69 (3) ◽  
pp. 830-836 ◽  
Author(s):  
M. C. Hogan ◽  
D. E. Bebout ◽  
A. T. Gray ◽  
P. D. Wagner ◽  
J. B. West ◽  
...  
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Hemoglobin Concentration ◽  
O2 Uptake ◽  
Isometric Twitch ◽  
O2 Delivery ◽  
Arterial Po2 ◽  
O2 Dissociation Curve ◽  
Total Hemoglobin Concentration

In the present study we investigated the effects of carboxyhemoglobinemia (HbCO) on muscle maximal O2 uptake (VO2max) during hypoxia. O2 uptake (VO2) was measured in isolated in situ canine gastrocnemius (n = 12) working maximally (isometric twitch contractions at 5 Hz for 3 min). The muscles were pump perfused at identical blood flow, arterial PO2 (PaO2) and total hemoglobin concentration [( Hb]) with blood containing either 1% (control) or 30% HbCO. In both conditions PaO2 was set at 30 Torr, which produced the same arterial O2 contents, and muscle blood flow was set at 120 ml.100 g-1.min-1, so that O2 delivery in both conditions was the same. To minimize CO diffusion into the tissues, perfusion with HbCO-containing blood was limited to the time of the contraction period. VO2max was 8.8 +/- 0.6 (SE) ml.min-1.100 g-1 (n = 12) with hypoxemia alone and was reduced by 26% to 6.5 +/- 0.4 ml.min-1.100 g-1 when HbCO was present (n = 12; P less than 0.01). In both cases, mean muscle effluent venous PO2 (PVO2) was the same (16 +/- 1 Torr). Because PaO2 and PVO2 were the same for both conditions, the mean capillary PO2 (estimate of mean O2 driving pressure) was probably not much different for the two conditions, even though the O2 dissociation curve was shifted to the left by HbCO. Consequently the blood-to-mitochondria O2 diffusive conductance was likely reduced by HbCO.(ABSTRACT TRUNCATED AT 250 WORDS)

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